When it comes to losing weight, pumping iron may be just as important as running on the treadmill, suggests a new study in the February issue of Cell Metabolism, a publication of Cell Press.
Researchers used a genetic trick in obese mice that caused the mice’s muscles to bulk up as though they had been lifting weights. The researchers found that the “genetically reprogrammed” mice lost fat and showed other signs of metabolic improvement throughout the body. What’s more, those benefits were seen even though the mice continued eating a diet high in both fat and sugar and didn’t increase their physical activity at all.
“We’ve shown that type II muscle does more than allow you to pick up heavy objects,” said Kenneth Walsh of Boston University School of Medicine. “It is also important in controlling whole-body metabolism.”
The type II, or fast, muscle fibers found plentifully in body builders are well suited to dealing with abrupt and heavy loads. On the other hand, the muscles of long-distance runners are rich in type I, or slow, fibers that can endure lesser loads over longer periods of time. Earlier studies focused primarily on the importance of type I muscle, with its abundance of energy-burning mitochondria, for regulating metabolism, Walsh said. Indeed, those studies have indicated that an increase in “energy burn” in muscle can protect against weight gain and metabolic dysfunction.
“Resistance training builds the white meat,” Walsh said, referring to the relatively mitochondria-poor type II muscle. “There is some evidence it’s good for you, but it’s not immediately clear why. Now, we’ve provided a scientific rationale.”
Walsh’s group developed mice in which they could turn type II muscle growth on or off by flipping a genetic switch specifically in skeletal muscle. The gene they manipulated, known as Akt1, is preferentially activated in skeletal muscle in response to resistance training, but not endurance training, the researchers knew.
Rather than becoming strong and fat “sumo mice” as some of the researchers had expected, the modified mice gained type II muscle and strength while they lost fat. The mice also showed a resolution of hepatic steatosis, otherwise known as fatty liver, and improvements in a variety of other metabolic parameters. The Akt1-driven growth of skeletal muscle counteracted the usual effects of a high-fat, high-sucrose diet on patterns of gene activity in the liver and increased the breakdown of fatty acids there, the researchers showed.
“These findings indicate that type II muscle has a previously unappreciated role in regulating whole-body metabolism through its ability to alter the metabolic properties of remote tissues,” the researchers concluded. “These data also suggest that strength training, in addition to the widely prescribed therapy of endurance training, may be of particular benefit to overweight individuals.”
“The work of [Walsh and his colleagues] reveals the intricate interplay between diet, energy balance, and the function/morphology of diverse tissue systems such as skeletal muscle and liver,” said Brooke Harrison and Leslie Leinwand of the University of Colorado at Boulder in a commentary. “These findings indicate that interventions designed to increase skeletal muscle mass in at-risk human populations may prove to be critical weapons in the fight against obesity and obesity-related comorbidities including diabetes, heart disease, stroke, hypertension, and cancer.”
The researchers include Yasuhiro Izumiya, Teresa Hopkins, Carl Morris, Kaori Sato, Ling Zeng, Jason Viereck, James A. Hamilton, Noriyuki Ouchi, Nathan K. LeBrasseur, and Kenneth Walsh, of Boston University School of Medicine, Boston, MA.